Thrombotic conditions such as myocardial infarction, stroke and pulmonary embolism all occur through formation, by platelet aggregation, of a platelet plug or thrombus. Knowledge gained in recent years with regard to the mechanism of platelet aggregation has led to the development of new drugs designed to treat thrombotic conditions by control of the platelet aggregation mechanism. More specifically, it is now known that the aggregation of human platelets in plasma occurs in two phases. The first phase is initiated by the presence of adenosine diphosphate (ADP) and is characterized by the clumping of platelets. The second phase, in which the platelets are irreversibly bound, is induced by the presence of arachidonic acid which is metabolized within the platelet to form Thromboxane A.sub.2 (TXA.sub.2) through certain endoperoxide intermediates in what has been termed the arachidonic acid cascade. TXA.sub.2 or certain endoperoxide intermediates, in turn, are believed to operate upon a receptor to effect platelet aggregation. Most work to date in this area has focused on reducing in vivo platelet reactivity (in the second phase) by specific inhibition of TXA.sub.2 synthesis or by blocking of the TXA.sub.2 /endoperoxide receptor.
The compound (I), 13-Azaprostanoic acid, is a known thromboxane A.sub.2 receptor antagonist and may be represented by the following formula: ##STR3##
Venton, Le Breton and Enke in U.S. Pat. No. 4,239,778 and in "Azaprostanoic Acid Derivatives. Inhibitors of Arachidonic Acid Induced Platelet Aggretation", J. Med. Chem. 1979, Vol. 22, No. 7, pp. 824-830 teach that certain azaprostanoic acid derivatives are potent inhibitors of platelet aggregation. In their literature article, Venton et al describe the only aryl compound which they tested, a 14-benzyl derivative, as being totally inactive.
In order to further elucidate the platelet aggregation process, various studies of the binding of thromboxane receptors have been conducted using tritium labelled 13-APA. However, the extent of these studies has been limited by the relatively low level of radioactivity of tritium and the weak potency of 13-APA. Accordingly, a need has existed for a more potent thromboxane receptor blocker which can be labelled with a more highly radioactive substance.